21. Motor Systems Flashcards
(281 cards)
1
Q
What is the collective term given to the basal ganglia and cerebellum?
A
Extrapyramidal system
2
Q
Broadly speaking, what is the role of the extra-pyramidal system?
A
- It checks that the movement selected by the motor cortex is correct
- They are responsible for the involuntary and automatic control of all musculature:
- Muscle tone
- Balance
- Posture
- Locomotion
- They are responsible for the involuntary and automatic control of all musculature:
- Both parts of the extrapyramidal system has functions aside from modulating motor control
3
Q
Where is the basal ganglion located?
A
White matter in the middle of the brain
4
Q
What are the different parts of the basal ganglia?
A
-
Striatum
- Caudate nucleus
- Putamen
-
Globus Pallidus
- External segment (GPext)
- Internal segment (GPint)
-
Substantia nigra
- Pars compacta (SNc)
- Pars reticulata (SNr)
- Subthalamic nucleus
5
Q
What is the function of the basal ganglia?
A
- It is involved in planning and coordinating movement
- It elaborates associated movements
- e.g. swinging arms when walking
- Contribute to the smoothness of complex action Involved in moderating and coordinating movements
6
Q
Describe the structure of the direct pathway in the basal ganglia.
A
Fibres initially come from the motor cortex to the striatum (caudate and putamen)
- Direct Pathway: putamen –> internal segment (GPi) + pars reticulata (SNr)
7
Q
Describe the structure of the indirect pathway in the basal ganglia.
A
- Fibres initially come from the motor cortex to the striatum (caudate and putamen)
- Putamen –> globus pallidus external segment –> subthalamic nucleus –> globus pallidus internal segment
8
Q
What is the difference in the function of the direct and indirect pathways?
A
- Direct Pathway = excitatory on the motor cortex
- Indirect Pathway = inhibitory on the motor cortex
9
Q
What extra component modulates the function of the direct and indirect pathways?
A
Nigro-striatal pathway
10
Q
Where do the projections go after leaving the basal ganglion structures?
A
- They go to the thalamus
- From the thalamus they go to the cortex
-
Primary motor area (BA4) and supplementary motor area (BA6)
- two regions involved in movement preparation and planning
-
Primary motor area (BA4) and supplementary motor area (BA6)
11
Q
Describe how the basal ganglia are involved in choosing correct motor programmes to carry out particular functions
A
- The basal ganglia and cortex form a processing loop
- The basal ganglia enable proper motor programmes (stored in the cortex) via the direct pathway (excitatory)
- The basal ganglia inhibit the competing motor programmes via the indirect pathway
- In summary, the basal ganglia and its direct and indirect pathways make sure that appropriate motor commands get transmitted down the hierarchy.
12
Q
Connections with which parts of the brain allow the basal ganglia to have a role in enabling various cognitive, executive and emotional programmes?
A
- Prefrontal cortex
- Limbic system
13
Q
What causes Parkinson’s disease?
A
- Parkinson’s disease is the neuronal degeneration of dopaminergic neurones in the pars compacta (SNc)
- It is caused by the progressive depletion of dopaminergic neurones
- NOTE: symptoms only appear when 80% of the dopamine cells in the substantia nigra have died
14
Q
What are the consequences of Parkinson’s with regards to the circuitry of the basal ganglia?
A
- The loss of nigro-striatal dopaminergic axons in the caudate and putamen mean that the connection between the striatum and pars compacta (SNc) is lost.
- Striatum = caudate nucleus and putamen
- This means that the direct pathway is reduced and so the excitation of the motor cortex is reduced
- The lack of excitatory input interferes with the ability of the motor cortex to generate commands for voluntary movement, resulting in poverty of movement.
15
Q
State the main signs of Parkinson’s disease.
A
-
Bradykinesia
- slow movement
-
Akinesia
- difficulty in the initiation of movements
-
Hypomimic face
- expressionless face
- Tremor
-
Rigidity
- increase in muscle tone
16
Q
Describe the Parkinsonian gait.
A
- Walking slowly
- Small steps
- Shuffling feet
- Reduced arm swing
- Stooped posture with head and body bent forwards and downwards
17
Q
What is Huntington’s disease caused by?
A
- Abnormality on chromosome 4 (autosomal dominant)
- Caused by the degeneration of GABAergic neurones in the striatum
- Firstly the caudate and then the putamen
18
Q
What are the consequences of Huntington’s disease with regards to the circuitry of the basal ganglia?
A
- The inhibitory effect of the indirect pathway no longer keeps the direct pathway under control so the cortex will be hyperexcitable
- Patients will continuously have abnormal movements because the cortex is continuously sending involuntary commands for movements
19
Q
What are the main signs of Huntington’s disease and how does the disease progress?
A
- Chorea = brief, semi-directed, irregular movements that are not repetitive or rhythmic, but appear to flow from one muscle to the next
- Choreic movements
- Rapid, jerky, involuntary movements of the body
- Hands and face are affected first
- Chorea gradually increases over time until the patients are totally incapacitated by it
- Later on the patients will develop cognitive decline and dementi
20
Q
State the 3 lobes of the cerebellum.
A
Anterior Posterior Flocculonodular
21
Q
The cerebellum is divided sagitally into 3 zones. What are these zones?
A
Vermis (midline) Intermediate hemisphere (closest to vermis) Lateral hemisphere
22
Q
State the 3 layers of the cerebellar cortex.
A
Granule cell layer Purkinje cells Molecular layer
23
Q
Name the 3 deep nuclei that are involved in the connections of thecerebellum with other parts of the body. Include their function.
A
Fastigial = involved in control of balance and connected with vestibular nuclei Interposed + Dentate = both involved in voluntary movement and are connected to the thalamus and the red nucleus
24
Q
What are the 3 sources of input into the cerebellum and what do they connect with?
A
Mossy Fibres – from the cortex and pons (corticopontine fibres) Mossy Fibres – from the spinocerebellar tract Climbing Fibres – from the inferior olive
25
Functionally, the cerebellum can be divided in three. What are these three divisions?
Vestibulocerbellum Spinocerebellum Cerebrocerebellum
26
What is the role of the vestibulocerebellum?
Vestibulocerbellum is the flocculonodular lobe It is connected to vestibular nuclei Involved in balance, posture and regulation of gait It is also involved in coordination of head movements with eye movements
27
Which parts of the cerebellum are part of the spinocerebellum?
Vermis and intermediate hemisphere
28
From where does the spinocerebellum receive inputs?
Afferents from axial portions of the body, visual, auditory and trigeminal inputs --\> vermis Afferents from limbs --\> intermediate hemisphere
29
What are the roles of the spinocerebellum?
Coordination of speech Adjustment of muscle tone Coordination of limb movement
30
Which part of the cerebellum is part of the cerebrocerebellum?
Lateral hemisphere
31
From where does the cerebrocerebellum receive inputs and what are its main functions?
It receives projections from the cortex Main functions are: Coordination of skilled movements Cognitive function Attention Processing of language Emotional control
32
In summary, what are the four main functions of the cerebellum?
Maintenance of balance and posture Coordination of voluntary movements Motor learning Cognitive functions
33
State three syndromes caused by dysfunction of different parts of the cerebellum.
Vestibulocerebellar syndrome/Flocculonodular lobe syndrome Spinocerebellar syndrome Cerberocerebellar syndrome
34
What are the symptoms of vestibulocerebellar syndrome?
This syndrome is similar to vestibular disease Patients tend to lose their balance with gait ataxia and a tendency to fall.
35
What behavioural habit is spinocerebellar syndrome associated with?
Chronic alcoholism
36
Describe the symptoms of spinocerebellar syndrome.
Mainly affects the legs It causes abnormal gait and a wide-based stance
37
Describe the symptoms of cerebrocerebellar syndrome.
Damage mainly affects the arms It affects coordinated movements Speech becomes very hesitant and slow (staccato)
38
What are the main signs of cerebellar disorders?
Ataxia– general impairments in movement coordination and accuracy Dysmetria– inappropriate force and distance for target-directed movements Intention tremor– increasingly oscillatory trajectory of a limb in a target directed movement (nose-finger tracking) Dysdiadochokinesia– inability to perform rapid alternating movements Scanning speech– staccato, due to impaired coordination of speech muscles
39
State a hereditary and acquired cause of the symptoms listed above.
Hereditary – Friedreich’s Ataxia Acquired – Multiple Sclerosis
40
What is volition?
Motor systems produce movements that are adaptive and accomplish a certain goal
41
Describe the hierarchical organisation of motor control.
Association Cortex Motor Cortex Brainstem Spinal Cord
42
What are postural adjustments and unconscious processing?
Postural Adjustments – the motor system has to compensate for changes in the body’s centre of mass during movements Unconscious Processing – many of the postural adjustments occur without our awareness
43
What are the three parts of the motor cortex?
Primary Motor Cortex Premotor Cortex Supplementary Motor Area
44
What is volition?
Motor systems produce movements that are adaptive and accomplish a certain goal
45
Describe the hierarchical organisation of motor control.
Association Cortex Motor Cortex Brainstem Spinal Cord
46
What are postural adjustments and unconscious processing?
Postural Adjustments – the motor system has to compensate for changes in the body’s centre of mass during movements Unconscious Processing – many of the postural adjustments occur without our awareness
47
What are the three parts of the motor cortex?
Primary Motor Cortex Premotor Cortex Supplementary Motor Area
48
What makes up the association cortex?
Frontal Cortex Parietal Cortex NOTE: this is not exactly part of the motor pathway but it influences the planning and execution of movements
49
What are the two parts of the pyramidal (descending) system?
Corticospinal Tract – starts in the cortex and exits and innervates the muscles in the arms and legs Corticobulbar Tract – starts in the cortex then exits and innervates the muscles in the face
50
Describe the side loops of this descending pathway and their role.
The descending pathway also has two side loops that go to the cerebellum and basal ganglia The cerebellum and basal ganglia check the motor information before ittravels to the muscles and has its effect
51
Which lobe are the three parts of the motor cortex found in? Describe their arrangement.
Frontal (anterior to the central sulcus) The primary motor cortex is on the precentral gyrus The premotor cortex and the supplementary motor area are anterior to the primary motor area
52
What is another name given to the three parts of the motor cortex?
Primary Motor Cortex = Broadmann’s Area 4 Premotor + Supplementary Motor Area = Broadmann’s Area 6
53
What are the most important cells in the primary motor cortex?
Betz Cells (pyramidal cells)
54
Where are these cells located within the grey matter and which tracts originate from here?
They are found in the 5th layer of grey matter The corticospinal tracts originate from here
55
Describe what happens to the upper motor neurones that come from the primary motor cortex.
They travel through the brainstem to the pyramidal decussation in themedulla where 90% of the axons cross the midline. These axons continue down the spinal cord and synapse with a lower motor neurone and exit into a peripheral nerve to the reach the skeletal muscle. The pathway of the corticobulbar tract is somewhat similar – upper motor neurones go down into the brainstem and synapse with a lower motor neurone and they exit to the muscles of the face
56
What are the two types of descending pathway?
Lateral and Medial
57
Which tracts fall into each of these types?
Lateral Lateral corticospinal tract Rubrospinal tract Medial Anterior corticospinal tract Reticulospinal tract Vestibulospinal tract Tectospinal tract
58
What is the function of each of these types of pathway?
Lateral Control of proximal and distal musculature Voluntary movements or arms and legs Medial Control of axial muscles Balance and posture
59
Describe the structure and function of the lateral corticospinal tract.
The lateral corticospinal tract originates in the primary motor cortex from the Betz cells. Their axons pass down through the brainstem and decussate at the pyramidal decussation in the medulla. It then passes down the spinal cord and synapses with a lower motor neurone. It goes onto control mainly the distal musculature. NOTE: 90% of axons from the primary motor cortex decussate at the medulla (these are the lateral corticospinal tract axons). The 10% that don’t decussate form the anterior corticospinal tract.
60
Where does the rubrospinal tract originate?
Red nucleus of the midbrain
61
What is the function of the rubrospinal tract?
It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex. It also has a role in movement velocity.
62
Describe the structure and function of the vestibulospinal tract.
The lateral vestibulospinal tract originates at the lateral vestibular nucleus. The medial vestibulospinal tract originates at the medial vestibular nucleus. They mediate postural adjustments and head and eye movements
63
Describe the structure and function of the reticulospinal tract.
It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle. It is involved in complex actions: Orienting Stretching Maintaining a complex posture
64
Describe the structure and function of the tectospinal tract.
It originates in the superior colliculus (brainstem) Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.
65
Describe the structure and function of the anterior corticospinal tract.
The anterior corticospinal tract is made up of the upper motor neurone axons coming from the primary motor cortex that do not decussate at the pyramidal decussation. These fibres cross the midline at the level of the spinal cord It controls proximal musculature.
66
What diagram depicts the somatotopic organisation of the primary motor cortex?
Penfield’s Motor Homunculus
67
How can the cortical representation of a muscle in the motor cortex change?
The more we use a muscle, the bigger the representation of that muscle in the cortex.
68
What is the function of the premotor cortex?
Plans movements and assembles movements into coordinated actions NOTE: premotor cortex is anterior to the primary motor cortex
69
What is the function of the supplementary motor area?
Planning complex internally driven voluntary movements e.g. speech It also becomes active when you are thinking about movement before movement (e.g. rehearsing a dance)
70
What are the two parts of the association cortex that are involved in motor control? State their functions.
Posterior Parietal Cortex – ensures movements are targeted accurately to objects in external space Prefrontal Cortex – involved in the selection of appropriate movements for a particular course of action
71
Describe the features of upper motor neurone lesions.
Initially you get loss of function of the motor neurones leading to: Paresis = graded weakness of movement Paralysis = complete loss of muscle activity After a few weeks, the loss of descending inhibitory pathways leads to increased abnormal motor activity such as: Spasticity (increased muscle tone) Hyperreflexia (exaggerated reflexes) Clonus (abnormal oscillatory muscle contraction) Babinski’s Sign NO muscle atrophy
72
What is Babinski’s Sign?
You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards) In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.
73
Why is muscle atrophy not seen in upper motor neurone lesions?
The lower motor neurones are still in tact and they have a role inproviding nutrients to the muscle. There will still be partial atrophy due to muscle disuse.
74
Define apraxia.
A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea). It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.
75
Lesions in which part of the brain tend to cause apraxia?
Inferior parietal lobe Frontal lobe (premotor cortex and supplementary motor area)
76
What are the two most common causes of apraxia?
Stroke and Dementia
77
Describe the features of lower motor neurone lesions.
It is generally the opposite of upper motor neurone lesions. Hypotonia Hyporeflexia Weakness Muscle Atrophy– the metabolic trophic support to the muscles is lost FASCICULATIONS– damages motor units produce spontaneous action potentials, resulting in a visible twitch Fibrillations – twitch of individual muscle fibres (aren’t visible to the naked eye but are picked up on EMG)
78
What is motor neurone disease?
A progressive neurodegenerative disorder of the motor system – it is a spectrum of disorders. MND can affect upper motor neurones, lower motor neurones or both
79
What is the term given for upper AND lower motor neurone disease?
Amyotrophic Lateral Sclerosis (ALS)
80
Describe how the symptoms of ALS change as the disease progresses.
Some patients may present with only upper motor lesion symptoms or only lower motor lesion symptoms but as the disorder progresses, both upper and lower motor neurone signs will be coexistent.
81
List some signs of ALS.
Increased muscle tone (spasticity in the limbs and tongue) Brisk limb and jaw reflexes (hyperreflexia) BABINSKI’s SIGN Loss of dexterity Dyarthria – difficulty speaking Dysphagia – difficulty swallowing
82
Which lower motor neurone controls the tongue?
Hypoglossal Nerve (CN XII)
83
What might you see in the tongue of an MND patient?
Fasciculations and spasticity
84
What makes up the association cortex?
Frontal Cortex Parietal Cortex NOTE: this is not exactly part of the motor pathway but it influences the planning and execution of movements
85
What might you see in the tongue of an MND patient?
Fasciculations and spasticity
86
Which lower motor neurone controls the tongue?
Hypoglossal Nerve (CN XII)
87
List some signs of ALS.
Increased muscle tone (spasticity in the limbs and tongue) Brisk limb and jaw reflexes (hyperreflexia) BABINSKI’s SIGN Loss of dexterity Dyarthria – difficulty speaking Dysphagia – difficulty swallowing
88
Describe how the symptoms of ALS change as the disease progresses.
Some patients may present with only upper motor lesion symptoms or only lower motor lesion symptoms but as the disorder progresses, both upper and lower motor neurone signs will be coexistent.
89
What is the term given for upper AND lower motor neurone disease?
Amyotrophic Lateral Sclerosis (ALS)
90
What is motor neurone disease?
A progressive neurodegenerative disorder of the motor system – it is a spectrum of disorders. MND can affect upper motor neurones, lower motor neurones or both
91
Describe the features of lower motor neurone lesions.
It is generally the opposite of upper motor neurone lesions. Hypotonia Hyporeflexia Weakness Muscle Atrophy– the metabolic trophic support to the muscles is lost FASCICULATIONS– damages motor units produce spontaneous action potentials, resulting in a visible twitch Fibrillations – twitch of individual muscle fibres (aren’t visible to the naked eye but are picked up on EMG)
92
What are the two most common causes of apraxia?
Stroke and Dementia
93
Lesions in which part of the brain tend to cause apraxia?
Inferior parietal lobe Frontal lobe (premotor cortex and supplementary motor area)
94
Define apraxia.
A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea). It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.
95
Why is muscle atrophy not seen in upper motor neurone lesions?
The lower motor neurones are still in tact and they have a role inproviding nutrients to the muscle. There will still be partial atrophy due to muscle disuse.
96
What is Babinski’s Sign?
You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards) In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.
97
Describe the features of upper motor neurone lesions.
Initially you get loss of function of the motor neurones leading to: Paresis = graded weakness of movement Paralysis = complete loss of muscle activity After a few weeks, the loss of descending inhibitory pathways leads to increased abnormal motor activity such as: Spasticity (increased muscle tone) Hyperreflexia (exaggerated reflexes) Clonus (abnormal oscillatory muscle contraction) Babinski’s Sign NO muscle atrophy
98
What are the two parts of the association cortex that are involved in motor control? State their functions.
Posterior Parietal Cortex – ensures movements are targeted accurately to objects in external space Prefrontal Cortex – involved in the selection of appropriate movements for a particular course of action
99
What is the function of the supplementary motor area?
Planning complex internally driven voluntary movements e.g. speech It also becomes active when you are thinking about movement before movement (e.g. rehearsing a dance)
100
What is the function of the premotor cortex?
Plans movements and assembles movements into coordinated actions NOTE: premotor cortex is anterior to the primary motor cortex
101
How can the cortical representation of a muscle in the motor cortex change?
The more we use a muscle, the bigger the representation of that muscle in the cortex.
102
What diagram depicts the somatotopic organisation of the primary motor cortex?
Penfield’s Motor Homunculus
103
Describe the structure and function of the anterior corticospinal tract.
The anterior corticospinal tract is made up of the upper motor neurone axons coming from the primary motor cortex that do not decussate at the pyramidal decussation. These fibres cross the midline at the level of the spinal cord It controls proximal musculature.
104
Describe the structure and function of the tectospinal tract.
It originates in the superior colliculus (brainstem) Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.
105
Describe the structure and function of the reticulospinal tract.
It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle. It is involved in complex actions: Orienting Stretching Maintaining a complex posture
106
Describe the structure and function of the vestibulospinal tract.
The lateral vestibulospinal tract originates at the lateral vestibular nucleus. The medial vestibulospinal tract originates at the medial vestibular nucleus. They mediate postural adjustments and head and eye movements
107
What is the function of the rubrospinal tract?
It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex. It also has a role in movement velocity.
108
Where does the rubrospinal tract originate?
Red nucleus of the midbrain
109
Describe the structure and function of the lateral corticospinal tract.
The lateral corticospinal tract originates in the primary motor cortex from the Betz cells. Their axons pass down through the brainstem and decussate at the pyramidal decussation in the medulla. It then passes down the spinal cord and synapses with a lower motor neurone. It goes onto control mainly the distal musculature. NOTE: 90% of axons from the primary motor cortex decussate at the medulla (these are the lateral corticospinal tract axons). The 10% that don’t decussate form the anterior corticospinal tract.
110
What is the function of each of these types of pathway?
Lateral Control of proximal and distal musculature Voluntary movements or arms and legs Medial Control of axial muscles Balance and posture
111
Which tracts fall into each of these types?
Lateral Lateral corticospinal tract Rubrospinal tract Medial Anterior corticospinal tract Reticulospinal tract Vestibulospinal tract Tectospinal tract
112
What are the two types of descending pathway?
Lateral and Medial
113
Describe what happens to the upper motor neurones that come from the primary motor cortex.
They travel through the brainstem to the pyramidal decussation in themedulla where 90% of the axons cross the midline. These axons continue down the spinal cord and synapse with a lower motor neurone and exit into a peripheral nerve to the reach the skeletal muscle. The pathway of the corticobulbar tract is somewhat similar – upper motor neurones go down into the brainstem and synapse with a lower motor neurone and they exit to the muscles of the face
114
Where are these cells located within the grey matter and which tracts originate from here?
They are found in the 5th layer of grey matter The corticospinal tracts originate from here
115
What are the most important cells in the primary motor cortex?
Betz Cells (pyramidal cells)
116
What is another name given to the three parts of the motor cortex?
Primary Motor Cortex = Broadmann’s Area 4 Premotor + Supplementary Motor Area = Broadmann’s Area 6
117
Which lobe are the three parts of the motor cortex found in? Describe their arrangement.
Frontal (anterior to the central sulcus) The primary motor cortex is on the precentral gyrus The premotor cortex and the supplementary motor area are anterior to the primary motor area
118
Describe the side loops of this descending pathway and their role.
The descending pathway also has two side loops that go to the cerebellum and basal ganglia The cerebellum and basal ganglia check the motor information before ittravels to the muscles and has its effect
119
What are the two parts of the pyramidal (descending) system?
Corticospinal Tract – starts in the cortex and exits and innervates the muscles in the arms and legs Corticobulbar Tract – starts in the cortex then exits and innervates the muscles in the face
120
What are the two enlargements in the spinal cord and what is their significance?
Cervical enlargement (C4-T1) – has extra motor neurons that go to the muscles of the upper limb Lumbosacral enlargement (L2-S3) – has extra motor neurons that go to the muscles of the lower limb
121
What are the little protrusion of pia mater around the spinal cord called?
Denticulate ligaments
122
Which space is present in the spinal meninges but not in the cranial meninges?
Epidural space – this can be used for injecting anaesthetics
123
What are the three most important tracts in spinal cord injury? State their roles.
Lateral corticospinal tract – fine motor movements Dorsal columns – touch, pressure, vibration, proprioception Spinothalamic tract – pain and temperature
124
What are the two stages of lateral corticospinal tract damage?
SPINAL SHOCK – you get loss of reflexes below the level of the lesion leading to flaccid paralysis. The limbs become floppy and there is little muscle tone RETURN OF REFLEXES – you get hyperreflexia and spasticity. The patient experiences spontaneous muscle contraction and there is very high muscle tone – rigid paralysis
125
Where do the upper motor neurons within the lateral corticospinal tract decussate?
Pyramidal decussation in the medulla
126
If you have a unilateral lesion of the lateral corticospinal tract in the mid-thoracic region, where will the deficit be?
Ipsilateral – on the same side as the lesion because the fibres decussate at the pyramidal decussation in the medulla
127
Where do the sensory fibres of the dorsal columns decussate?
Sensory decussation in the medulla
128
How are pain neurons arranged differently to other sensory and motor neurons?
The first order neurons synapse in the dorsal horn and then the second order neuron crosses to the contralateral side immediately (at the level of the synapse with the first order neurone) The second order neurons then ascend on the contralateral side
129
What is syringomyelia? Describe and explain its features.
Enlargement of the central canal (the space is called a syrinx) This selectively affects the spinothalamic fibres that are crossing at the level of the lesion and it does not affect fibres that have alreadycrossed So if the enlargement of the central canal is in the region of the cervical enlargement, you could get loss of pain/temperature sensation in the arms but not the legs (because those fibres would already have crossed and would be ascending in the spinothalamic tract away from the central canal)
130
Spinothalamic anterior
-consicous sensation -crude touch, pressure first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus-third order neurons synapse in primary sensory cortex
131
Spinothalamic lateral
-consicous sensation -pain, temperature -first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus -third order neurons synapse in primary sensory cortex
132
Posterior column
-consicous sensation -fine touch, pressure, vibration, proprioreception -first order synapses at the medulla -decussates at the medulla -second order synapses in thalamus -third order synapses with primary sensory cortex
133
Spinocerebellar posterior
-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -NO decussation second order synapse at cerebellum -NO 3rd order
134
Spinothalamic anterior
-consicous sensation -crude touch, pressure first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus-third order neurons synapse in primary sensory cortex
135
Spinothalamic lateral
-consicous sensation -pain, temperature -first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus -third order neurons synapse in primary sensory cortex
136
Posterior column
-consicous sensation -fine touch, pressure, vibration, proprioreception -first order synapses at the medulla -decussates at the medulla -second order synapses in thalamus -third order synapses with primary sensory cortex
137
Spinocerebellar posterior
-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -NO decussation second order synapse at cerebellum -NO 3rd order
138
Spinocerebellar anterior
-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -DECUSSATION -second order (interneurons) synapse at cerebellum -NO 3rd order
139
Spinocerebellar anterior
-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -DECUSSATION -second order (interneurons) synapse at cerebellum -NO 3rd order
140
What is the morphology of somatic sensory neurons?
Pseudounipolar - they do not have any dendrites
141
What is the equivalent of astrocytes in the PNS?
Satellite cells
142
Describe the packaging of nerve axons into larger structures.
Axons are packaged into fascicles and the fascicles are packaged into nerves.
143
What are the three layers of connective tissue found in nerves?
Endoneurium - wraps around individual axons Perineurium - wraps around fascicles Epineurium - wraps around nerves REMEMBER: unmyelinated axons also have Schwann cells wrapped around them, the difference is that they only have one layer of membrane around them and one Schwann cell can accommodate many axons.
144
Describe the arrangement of autonomic motor neurons.
Autonomic motor neurons have a preganglionic neuron and a postganglionic neuron with an autonomic ganglion in the middle. The location of the autonomic ganglion varies depending on whether it is sympathetic or parasympathetic.
145
Which roots do motor and sensory nerves go out of?
Motor = ventral Sensory = dorsal
146
Where do autonomic sensory neurons have their cell bodies?
In the dorsal root ganglion
147
What is a myotome?
The muscle that a spinal nerve innervates
148
What spinal nerves make up the brachial plexus?
C5-T1
149
What are the nerves called that are leaving the brachial plexus?
Peripheral nerves
150
Describe the differences in the dermatomes of spinal nerves and peripheral nerves.
Spinal nerves = stripey Peripheral nerves = patchy
151
Describe the process of regeneration following peripheral nerve injury.
With compression injuries, the axoplasm is separated but the endoneurium is still in tact. The axon distal to the compression (further away from the cell body) degenerated - macrophages invade and phagocytose the cell debris. Axons sprouts then grow down the endoneurium. There is competition between the axonal sprouts to reach the target organ. When the first axon sprout reaches the target cell, the other axon sprouts regress. The axon then widens and a myelin sheath forms. The only difference is that the internodal distance is reduced so the conduction speed is reduced.
152
What could happen if the damage to the neuron is so severe that there are no guidance cues at all for the axonal sprouts?
A neuroma could form which is very painful and needs to be surgically removed.
153
What are the two types of peripheral neuropathy? Describe them.
Segmental Demyelination - loss of a Schwann cell hear and there. This will not kill the cell but it will slow down the action potential. Axonal Degeneration - once you already have degeneration of an axon, the myelin also degenerates and you get a conduction block
154
What are two techniques of diagnosing peripheral neuropathy?
Conduction velocity Nerve biopsy
155
What are the three main dopaminergic pathways in the brain?
Nigrostriatal Mesolimbic Tuberoinfundibular system
156
Where are each of these pathways found?
Nigrostriatal– projecting from the substantia nigra pars compacta to the striatum Mesolimbic– projecting from the ventral tegmental area to the nucleus accumbens, frontal cortex, limbic cortex and olfactory tubercle Tuburoinfundibular system– projecting from the arcuate nucleus in the hypothalamus to the median eminence and pituitary gland
157
What are the roles of these pathways?
Nigrostriatal – control of movement Mesolimbic – involved in emotion Tuburoinfundibular system – regulate hormone secretion
158
What are the two families of dopamine receptors and which receptors fall into each of these families?
D1 family – D1 + D5 D2 family – D2, D3 + D4
159
Describe dopamine synthesis.
Tyrosine is converted by tyrosine hydroxylase to DOPA DOPA is converted by DOPA decarboxylase to Dopamine
160
Is Parkinson’s disease more common in males or females?
Males – 4:1
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What percentage of all cases of Parkinson’s disease is accounted for by familial Parkinson’s disease?
8% The rest are idiopathic
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What are the possible causes of idiopathic Parkinson’s disease?
Possibly a combination of environmental, oxidative stress, altered protein metabolism and risk genes
163
What are the cardinal signs of Parkinson’ disease?
Resting tremor (pill-rolling tremor) Rigidity (stiffness – limbs feel weak and heavy) Bradykinesia (slowness of movement) Postural abnormality
164
What are the presenting symptoms of Parkinson’s disease?
Pill-rolling resting tremor Difficulty with fine movements (micrographia) Poverty of blinking Hypomimic face Monotony of speech and loss of volume of voice Disorders of posture – flexion of the neck and trunk Lack of arm swing Loss of balance – lack of righting reflex, retropulsion Short steps, shuffling gait
165
Describe the initial distribution of symptoms across the body.
Unilateral onset Symptoms spread to both sides Generally symptoms worsen with some patients becoming severely disabled
166
What are some non-motor symptoms of Parkinson’s disease?
Depression Pain Taste/smell disturbances Cognitive decline/dementia Autonomic dysfunction (constipation, postural hypotension, urinary frequency/urgency, impotence, increased sweating)
167
What is the main area of the brain that is affected by Parkinson’s disease?
Substantia nigra Other brain areas affected: locus coeruleus, dorsal vagus nucleus, nucleus basalis of Mynert
168
Describe the neuropathology of Parkinson’s disease.
Putamen-projecting pathways degenerate significantly Lewy bodies (large circular structure with bright core and white surrounding, packed with alpha-synuclein) also present – this is probably a defensive mechanism to protect against toxic altered proteins
169
What are the stages of Parkinson’s disease?
1-2 = dorsal motor nucleus of vagus, raphe nucleus, locus coeruleus 3 = substantia nigra pars compacta 4 = amygdala, nucleus of Meynert, hippocampus 5-6 = cingulate cortex, temporal cortex, frontal cortex, parietal cortex, occipital cortex
170
What is the main biochemical change seen in Parkinson’s disease?
Marked reduction in the caudate nucleus/putamen dopamine content
171
What proportion of dopaminergic neurones of the nigrostriatal dopaminergic pathway must be lost before symptoms occur?
80-85% of dopaminergic neurones and 70% of striatal dopamine must be depleted before symptoms appear
172
What is the reason for this?
There are compensatory mechanisms e.g. neurone overactivity and increase in dopamine receptors
173
What other type of drug has to be given with L-DOPA in dopamine replacement therapy and why?
Peripheral DOPA decarboxylase inhibitor This prevents the conversion of L-DOPA to dopamine by peripheral DOPA decarboxylase (this can cause nausea and vomiting)
174
State two different preparation of dopamine replacement therapy.
Sinamet = Carbodopa + L-DOPA Madopar = Benserazide + L-DOPA
175
What does L-DOPA treat?
Hypokinesia Tremor Rigidity
176
Describe how the dosage of L-DOPA is changed with continued treatment.
It is started low and increased until maximum benefit of drug is achieved without side effects Effectiveness of L-DOPA declines with time
177
What are the acute side effects of L-DOPA?
Nausea (prevented by domperidone) Hypotension Psychological effects (schizophrenia like syndrome with dellusions, hallucinations, confusion, disorientation and nightmares)
178
What are the chronic side effects of L-DOPA?
Dyskinesias (abnormal movement of limbs and face – can occur within 2 years of treatment – disappear with reduced dose) Rapid fluctuations in clinical state (off periods may last for minutes to hours
179
Name three dopamine agonists.
Bromocriptine Ropinerol Pergolide
180
Which receptors do they act on?
D2 receptor
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What are the benefits of dopamine agonists over L-DOPA?
Longer duration of action Smoother and more sustained response Actions independent of dopaminergic neurones Incidence of dyskinesias is less NOTE: L-DOPA is still the gold standard
182
What are the adverse effects of dopamine agonists?
Common – confusion, dizziness, nausea/vomiting, hallucinations Rare – constipation, headache, dyskinesia
183
What structure used to be present in older dopamine agonists that caused quite serious clinical problems?
Ergot ring This caused problems with heart valves
184
What has been the consequence of the removal of this structure within dopamine agonists?
Development of addictive behaviour e.g. gambling
185
Name two MAO inhibitors.
Deprenyl (selegiline) Rasagiline
186
What are the effects of Deprenyl?
Selective for MAO-B (this predominates in dopaminergic areas of CNS) Does NOT have the peripheral side effects of non-selective MAO inhibitors Can be given in combination with L-DOPA (reduce dose of L-DOPA by 30-50%)
187
What are the side effects of Deprenyl?
RARE Hypotension Nausea/vomiting Confusion and agitation
188
What are the effects of Rasagiline?
It has neuroprotective properties by inhibiting apoptosis (promotes anti-apoptosis genes) NOTE: early clinical trials show this drug might slow down the progression of disease but subsequent studies haven’t been so promising
189
Name two COMT inhibitors.
Tolocapone (CNS + PNS) Entacapone (PNS)
190
What are the effects of COMT inhibition in the CNS?
Prevents breakdown of dopamine in the brain
191
What are the effects of COMT inhibition in the peripheral nervous system?
Peripheral COMT converts L-DOPA to 3-O-methyl DOPA (3-OMD) 3-OMD competes with L-DOPA for the transport system that transports it across the BBB COMT inhibitors stop 3-OMD production and hence there is less competition for L-DOPA Result: REDUCE L-DOPA DOSAGE
192
What are the side effects of COMT inhibitors?
Cardiovascular complications
193
What percentage of the general population is affected by schizophrenia?
1%
194
What are the symptoms of schizophrenia?
Positive Symptoms (overt symptoms that should NOT be present) Hallucinations Delusions Disorganised thoughts Negative Symptoms (lack of characteristics that SHOULD be present) Reduced speech Lack of emotional and facial expression Diminished ability to begin and sustain activity Decreased ability to find pleasure in everyday life Social withdrawal Cognitive deficits Memory Attention Planning Decision making
195
What appears to have quite a strong contribution to the development of schizophrenia?
Genetics
196
Once schizophrenia has been diagnosed, what are the four main outcomes for patients?
1 – illness resolves completely, with or without treatment and never returns (10-20%) 2 – illness recurs repeatedly with full recovery between episodes (30-35%) 3 – illness recurs repeatedly with incomplete recovery and a persistent defective state develops, becoming more profound with each successive relapse (30-35%) 4 – illness pursues down a downhill course from the beginning (10-20%) NOTE: most cases are relapsing and remitting
197
Describe the involvement of dopamine in schizophrenia.
Positive symptoms – results from excessive dopamine transmission in the mesolimbic and striatal region (D2-mediated) Negative symptoms – results from dopamine deficit in the pre-frontal region (D1-mediated)
198
What evidence has arisen that supports this hypothesis?
Dopamine agonists can induce various psychotic reactions Typical antipsychotics are dopamine receptor antagonists (blocking D2 receptors)
199
Describe the involvement of glutamate in schizophrenia.
NMDA is a glutamate receptor Glutamate exerts an excitatory influence over the GABA-ergic striatal neurones and dopamine exerts an inhibitory influence These GABA-ergic striatal neurones project to the thalamus and constitute a sensory ‘gate’ Too little glutamate or too much dopamine disables this gate, allowing uninhibited sensory input to reach the cortex NOTE: you find reduced glutamate concentration and reduced glutamate receptors in post-mortem schizophrenic brains. Also NMDA receptor antagonists can produce psychotic symptoms
200
What is the most robust gene associated with schizophrenia?
Neuregulin-1
201
What are all the susceptibility genes for schizophrenia associatedwith?
Dopamine and glutamate neurotransmission
202
What type of drug are all neuroleptics?
Dopamine receptor antagonists (D2 receptors) NOTE: most neuroleptics block other receptors
203
Which symptoms do neuroleptic drugs treat?
Positive symptoms ONLY
204
What are the initial effects of neuroleptic drugs?
Initial increase in dopamine synthesis and neuronal activity – this declines with time
205
What is meant by an atypical antipsychotic?
Newer antipsychotics are given this term – they have fewer extrapyramidal side effects
206
Name an atypical antipsychotic.
Clozapine
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Name a typical antipsychotic.
Haloperidol
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What is an important other action of neuroleptics?
Anti-emetic Because they block dopamine receptors in the chemotactic trigger zone Phenothiazine is a neuroleptic that is really good at preventingnausea/vomiting caused by drugs NOTE: many neuroleptics also block histamine receptors – this is effective at controlling motion sickness
209
What are the extrapyramidal side effects of antipsychotics caused by?
Blockade of dopamine receptors in the nigrostriatal system can induce Parkinson-like side effects
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What are the two main extra-pyramidal side effects? Acute Dystonia
Involuntary movements Muscle spasm, protruding tongue, fixed upward gaze, neck spasm etc. Often accompanied by Parkinson’s like features Occur in the FIRST FEW WEEKS and often decline with ongoing therapy Reversible with withdrawal of the drug or anti-cholinergics Tardive Dyskinesias Involuntary movements Involving the face and tongue, but also trunk and limbs Occur in 20% of patients after SEVERAL MONTHS/YEARS of therapy Made WORSE by drug withdrawal or anti-cholinergics
211
What are the unwanted effects of antipsychotics?
Endocrine effects – loss of inhibition of prolactin secretion leads to hyperprolactinaemia (can lead to breast swelling and sometimes lactation) Blocking alpha-adrenoceptors – postural hypotension Blocking 5-HT receptors – weight gain Blockade of muscarinic receptors – typical anti-muscarinic effects e.g. blurring of vision, increased intra-ocular pressure, dry mouth, constipation, urinary retention
212
What test is used to see if someone has peripheral neuropathy?
Monofilament test
213
What is the most common site of ulcers on the foot?
Ball of the foot
214
What three arms of neuropathy are involved in causing foot ulceration and how are they involved? Motor Sensory Autonomic
Motor– causes imbalance between extensors and long plantar flexors causing an abnormal shape of the foot. This means there will be increased pressure being applied on the ball of the foot and knuckles ofthe toes. Sensory Autonomic– can lead to abnormal blood flow (increase pulse pressure in the foot). It also reduces sweating, which normally protects the foot from minor disease.
215
What effect can sugar binding to haemoglobin have on the feet?
Makes the tendons less flexible – limits joint mobility
216
What are the three types of diabetic feet?
Neuropathic Foot Ischaemic Foot Neuro-ischaemic Foot
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Describe the neuropathic foot. Where is the most common site of ulceration in these feet?
Numb Warm (because blood flow isn’t regulated properly) Dry Palpable foot pulses Ulcers – at points of high-pressure loading
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Describe the ischaemic foot. Where is the most common site of ulceration in these feet?
Cold Pulseless Ulcers – at foot margins
219
What is Charcot foot?
The neuropathy leads to joint overuse and misuse This leads to bones losing their normal articulations The abnormal foot shape makes it at extreme risk of ulceration
220
What can ulceration of the foot lead to?
Osteomyelitis
221
State the three main sites of microvascular complications.
Retinal arteries (retinopathy) Glomerular arterioles (nephropathy) Vasa vasorum (neuropathy)
222
What factors correlate with risk of microvascular and macrovascular complications?
Glycaemic control (HbA1c) Hypertension Other factors such as glycaemic memory and genetics can contribute
223
Describe the mechanism of glucose damage to blood vessels.
Hyperglycaemia leads to oxidative stress and hypoxia This triggers an inflammatory cascade, which leads to damage
224
What instrument is used to look into the eye?
Fundoscope
225
Where is the optic disc relative to the macula on the back of the eye?
The optic disc is nasal to the macula
226
What are the 4 types of diabetic retinopathy?
Background Pre-proliferative Proliferative Maculopathy
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What three features do you see in background diabetic retinopathy?
Hard exudates Microaneurysms Blot haemorrhages
228
What are hard exudates caused by?
Leakage of lipid contents makes the back of the eye look a cheesy colour
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Describe pre-proliferative diabetic retinopathy.
Soft exudates (cotton wool spots) There will be some haemorrhages
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What do soft exudates indicate?
Retinal ischaemia
231
Describe proliferative diabetic retinopathy.
Involves the formation of new vessels (in response to retinal ischaemia) The new vessels are generally more fragile and can bleed at any time
232
Describe maculopathy.
Presence of hard exudates in the macula This is the same disease as background diabetic retinopathy, it’s just that the hard exudates are in the macula This can threaten direct vision
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What are the steps taken in managing background diabetic retinopathy?
Improve blood glucose control
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What is the treatment for pre-proliferative and proliferative diabetic retinopathy?
Pan-retinal photocoagulation
235
Describe the treatment of maculopathy.
You need a grid of photocoagulation in the affected area (aim to limit damage to the macula so you don’t do pan-retinal photo coagulation)
236
State some histological features of diabetic nephropathy.
Mesangial expansion Basement membrane thickening Glomerulosclerosis (hardening of the capillaries)
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In diabetic nephropathy you get over production of matrix. Whatcan this be caused by?
Effects of prolonged exposure to high glucose or glycosylated proteins A rise in pressure within the glomerular capillaries Angiotensin II
238
State 3 clinical features of diabetic nephropathy.
Progressive proteinuria Increased blood pressure Deranged renal function
239
What is the normal range for proteinuria?
\< 30 mg/24hr
240
Why do patients with diabetic nephropathy get oedematous?
Increased proteinuria means that they are losing albumin through their urine This decreases serum albumin hence decreases the osmotic potential of the plasma so less fluid is drawn back into the circulation
241
Describe some strategies for intervention of patients with diabetic nephropathy.
Improve blood glucose control Blood pressure control Inhibition of the activity of the renin-angiotensin system Stopping smoking
242
What effect does angiotensin II have on endothelial cells?
It makes endothelial cells more rigid
243
Where is renin produced?
Juxtaglomerular apparatus
244
What can stimulate renin release?
Low renal perfusion (i.e. low blood pressure)
245
Where is ACE found?
Lungs
246
State some drug target sites in the renin-angiotensin system.
Drugs blocking renin activity ACE inhibitors Angiotensin II receptor blockers (ARBs)
247
What causes diabetic neuropathy?
Occlusion of the vasa vasorum
248
State 6 different types of diabetic neuropathy.
Peripheral polyneuropathy Mononeuropathy Mononeuritis multiplex Radiculopathy Autonomic neuropathy Diabetic amyotrophy
249
What can peripheral neuropathy lead to and how can it be tested?
Loss of sensation can lead to damage going unnoticed It also leads to loss of ankle jerks and loss of vibrational sense Inappropriate use of joints can lead to Charcot joints Test – monofilament examination
250
What is mononeuropathy?
Usually sudden motor loss e.g. wrist drop or foot drop Can also cause cranial nerve palsy
251
Why is the pupil spared in pupil sparing third nerve palsy?
The parasympathetic fibres, that are responsible for the diameter of the pupil, run on the outside of the main nerve so they don’t lose their blood supply in diabetes
252
How would an aneurysm causing third nerve palsy present differently to third nerve palsy caused by diabetes?
There would be fixed pupil dilation This is because the parasympathetic fibres would also be affected
253
What is mononeuritis multiplex?
A random combination of peripheral nerve lesions
254
What is radiculopathy?
Pain over SPINAL nerves Usually affecting a dermatome on the abdomen or chest wall
255
What are the effects of autonomic neuropathy on the GI tract?
Difficulty swallowing Delayed gastric emptying Constipation/nocturnal diarrhoea NOTE: it can also lead to bladder dysfunction
256
What are the effects of autonomic neuropathy on the CVS?
Postural hypotension There have been reports of sudden cardiac death
257
How can you check for autonomic neuropathy?
Measure changes in heart rate due to Valsalva manoeuvre Look at an ECG and compare the R-R intervals
258
What four factors affect the force generation in muscle contraction?
Recruitment of motor units Filament overlap Velocity and direction of movement Frequency of stimulus
259
What is a motor unit?
One motor neuron and all the muscle fibres it innervates
260
What happens if all the motor units are recruited for muscle contraction?
You get maximum voluntary contraction (MVC)
261
Where are lower motor neurons found?
In the anterior horn of the grey matter
262
What is a tetanus?
Prolonger contraction of a muscle due to rapidly repeated stimuli
263
What causes unfused tetanus?
If the frequency is not high enough for fused tetanus - there is enough time in between action potentials for the force of contraction to drop slightly before the next action potential causes the next contraction.
264
What is the difference between concentric and eccentric contraction?
Eccentric contraction generates more force
265
How does velocity and direction of movement affect force of contraction?
The greater the velocity the lower the force of contraction
266
Why is ATP needed for in muscle contraction?
ATP is needed for the detachment of myosin from actin ATP is also needed for the reabsorption of calcium into the sarcoplasmic reticulum
267
What hydrolyses phosphocreatine and how much ATP does this generate?
Creatine Phosphokinase 1 ATP
268
Why is tetanus not possible in cardiac muscle?
There is a very long absolute refractory period meaning that the once the heart muscle is available to be restimulated, it is already quite a long way through the contraction process.
269
Describe the excitation-contraction coupling of smooth muscle.
Depolarisation causes the opening of voltage gated calcium channels so calcium ions move into the cell. The calcium ions bind to calmodulin and form a Ca-CaM complex. The Ca-CaM complex activates myosin light chain kinase (MLCK), which then phosphorylates myosin light chains and leads to contraction.
270
The axons from which cells int eh motor cortex form the corticospinal and corticobulbar tracts?
Pyramidal cells
271
How do the coritcospinal and corticobulbar tracts descend from the motor cortex to the brainstem?
* Via the corona radiata, internal capsule and cerebral peduncle
272
How do upper motor neurone (UMN) syndromes arise?
* When the **descending motor pathways** are damaged at the level of the motor cortex or at any point of the descending pathway prior to the final synaps eiwth the motor neurones of the spinal cord or cranial enrve nculei
273
How do lower motor neurone syndromes arise?
* When damage occurs at the level of the motor neurones in the ventral horn of the spinal cord
* In the case of the spinal cord, this menas damage to the ventral roots and peripheral nerves leding to the muscles
274
What will a subcortical lesion (tumor, hematoma, infarct etc) result in?
Contralateral paresis of hand or arm.
275
What will a internal capsule lesion reuslt in?
Contralateral spastic hemiplagia
276
What will a peduncle lesion result in?
* Contralateral spastic hemiplegia, which may be associated with ipsilateral paralysis of the oculomotor nerve - Weber syndrome.
277
What will a pons lesion result in?
Contralateral and possibly bilateral hemiplegia.
278
What will a pyramidal lesion result in?
Flaccid contralateral hemiparesis
279
What will a cervical lesion result in?
Ipsilateral spastic hemiplegia
280
What will a thoracic lesion result in?
Unilateral: Spastic ipsilateral monoplegia. Bilateral: Spastic paraplegia.
281
What will an anterior root lesion result in?
The palsy resulting from this lesion is ipsilateral and flaccid as a result of the damage of the peripheral of lower motoneurons.
